E-GEOD-87643
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-87643 | ExpressionAtlas | 2020-04-06
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-87643-analysis-methods.tsv | Tabular | |||
| E-GEOD-87643-analytics.tsv | Tabular | |||
| E-GEOD-87643-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-87643-configuration.xml | Xml | |||
| E-GEOD-87643-g21_g1-mvaPlot.png | Other |
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Project description:O antigen acts as a shield to delay early plant immune recognition of the pathogenic bacterium, Xylella fastidiosa
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Project description:Fungal interactions with plant roots, either beneficial or detrimental, have a major impact on agriculture and ecosystems1. The soil inhabiting ascomycete Fusarium oxysporum (Fo) constitutes a species complex of worldwide distribution causing vascular wilt in more than a hundred different crops2,3. Individual isolates of the fungus exhibit host-specific pathogenicity, determined by proteinaceous effectors termed secreted in xylem (SIX)4,5. However, such isolates can also colonize roots of non-host plants asymptomatically as endophytes, or even protect the plant against pathogenic isolates6,7. The molecular determinants of multi-host plant colonization are currently unknown. Here, we identified a set of fungal effectors termed ERCs (Early Root Compatibility effectors), which are secreted during early biotrophic growth of Fo on both host and non-host plants. In contrast to SIX effectors, which are encoded on lineage specific (LS) genomic regions5,8, ERCs are encoded on core genomic regions and broadly conserved across the Fo species complex. Targeted deletion of ERC genes in pathogenic Fo isolate resulted in reduced virulence on the host plant and rapid activation of plant immune responses, while in a non-pathogenic isolate it led to impaired root colonization and loss of biocontrol ability. Strikingly, some ERCs also contribute to Fo infection on the non-vascular land plant Marchantia polymorpha. Our results reveal an evolutionarily conserved mechanism for multi-host colonization by root infecting fungi.
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Project description:PAMP-triggered immunity (PTI) is the first line of plant defense against invading organisms. Initiated through the perception of conserved pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide or flagellin, PTI can provide early protection against a broad range of pathogens. Active suppression of PTI by microbial effector proteins, particularly those secreted by the Type III secretion system (T3SS), is a well-known strategy employed by bacterial plant pathogens that enables them to subvert PTI and successfully colonize their hosts. In this study, we demonstrate that the xylem-limited bacterium, Xylella fastidiosa, which lacks a T3SS, utilizes an alternative strategy to delay elicitation of innate immune responses. By decorating its LPS PAMP molecule with a high molecular weight O antigen, this bacterium physically masks itself from early recognition by the grapevine innate immune system. We have elucidated the chemical structure of the O antigen and found that it is primarily an α1,2-linked rhamnan polymer. X. fastidiosa cells lacking O antigen elicited hallmarks of PTI such as ROS production, specifically in the plant xylem tissue compartment, which is comprised primarily of non-living cells. By coupling histological and genome-wide transcriptional profiling, we demonstrate that X. fastidiosa lacking its O antigen shield activates defense-related genes in grapevine. This includes a stronger and more prolonged oxidative burst at concentrations high enough to inhibit pathogen proliferation. To begin exploring translational applications of our findings, we also demonstrate that purified X. fastidiosa LPS elicitor can prime grapevine defenses, thereby conferring host tolerance to subsequent challenge with X. fastidiosa.
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Helicobacter pylori colonizes half of the world's population as the dominant member of the gastric microbiota resulting in a lifelong chronic infection. Host responses toward the bacterium can result in asymptomatic, pathogenic or even favorable health outcomes; however, mechanisms underlying the dual role of H. pylori as a commensal versus pathogenic organism are not well characterized. Recent evidence suggests mononuclear phagocytes are largely involved in shaping dominant immunity during infection mediating the balance between host tolerance and succumbing to overt disease. We combined computational modeling, bioinformatics and experimental validation in order to investigate interactions between macrophages and intracellular H. pylori. Global transcriptomic analysis on bone marrow-derived macrophages (BMDM) in a gentamycin protection assay at six time points unveiled the presence of three sequential host response waves: an early transient regulatory gene module followed by sustained and late effector responses. Kinetic behaviors of pattern recognition receptors (PRRs) are linked to differential expression of spatiotemporal response waves and function to induce effector immunity through extracellular and intracellular detection of H. pylori. We report that bacterial interaction with the host intracellular environment caused significant suppression of regulatory NLRC3 and NLRX1 in a pattern inverse to early regulatory responses. To further delineate complex immune responses and pathway crosstalk between effector and regulatory PRRs, we built a computational model calibrated using time-series RNAseq data. Our validated computational hypotheses are that: 1) NLRX1 expression regulates bacterial burden in macrophages; and 2) early host response cytokines down-regulate NLRX1 expression through a negative feedback circuit. This paper applies modeling approaches to characterize the regulatory role of NLRX1 in mechanisms of host tolerance employed by macrophages to respond to and/or to co-exist with intracellular H. pylori.
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